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首页> 外文期刊>Cell communication & adhesion >Connexin26 Regulates the Expression of Angiogenesis-Related Genes in Human Breast Tumor Cells by Both GJIC-Dependent and -Independent Mechanisms
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Connexin26 Regulates the Expression of Angiogenesis-Related Genes in Human Breast Tumor Cells by Both GJIC-Dependent and -Independent Mechanisms

机译：连接蛋白26通过GJIC依赖性和非依赖性机制调节人乳腺肿瘤细胞中血管生成相关基因的表达。

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We previously reported that over-expression of connexins in mammary tumor cells retarded tumor growth in vivo in the absence of appreciable gap junction formation, highlighting a possible connexin-linked, but gap junctional intercellular communication (GJIC)-independent mechanism. In the current study, we engineered GJIC-deficient MDA-MB-435 human breast tumor cells to express a chimeric Cx26 where the green fluorescent protein was fused to the amino-terminal of Cx26 (GFP-Cx26). Characterization of this chimeric protein revealed that GFP-Cx26 assembled into non-functional gap junction-like clusters that were impermeable to Lucifer Yellow. In contrast, expression of wild-type Cx26 or Cx26 tagged at the carboxy terminal with yellow fluorescent protein, efficiently rescued GJIC in these tumor cells. Interestingly, by screening 96 tumor-related genes, we observed that the expression of Cx26 or GFP-Cx26 in the tumor cells up-regulated both the transcription and the translation of thrombospondin-1 (TSP-1), an anti-angiogenic molecule. Affymetrix array analysis extended the list of Cx26 or GFP-Cx26 regulated genes by ten candidates including connective tissue growth factor (CTGF), another angiogenesis-related gene. CTGF mRNA and protein levels were found to be down-regulated by both Cx26 and GFP-Cx26. Thus, our data indicates that Cx26 regulates angiogenesis-related molecules by mechanisms that are both GJIC-dependent and -independent.
机译：我们以前曾报道过，在没有明显的间隙连接形成的情况下，乳腺肿瘤细胞中连接蛋白的过度表达会抑制体内肿瘤的生长，从而突显出可能存在连接蛋白连接但间隙连接的细胞间通讯（GJIC）独立机制。在本研究中，我们改造了GJIC缺失的MDA-MB-435人乳腺肿瘤细胞，以表达嵌合的Cx26，其中绿色荧光蛋白融合到Cx26的氨基末端（GFP-Cx26）。对该嵌合蛋白的表征表明，GFP-Cx26组装成不可渗透的荧光素黄的无功能间隙连接样簇。相反，在羧基末端标记有黄色荧光蛋白的野生型Cx26或Cx26的表达有效地拯救了这些肿瘤细胞中的GJIC。有趣的是，通过筛选96个与肿瘤相关的基因，我们观察到肿瘤细胞中Cx26或GFP-Cx26的表达上调了抗血管生成分子血小板反应蛋白1（TSP-1）的转录和翻译。 Affymetrix阵列分析通过十个候选对象扩展了Cx26或GFP-Cx26调控的基因列表，其中包括结缔组织生长因子（CTGF），另一个与血管生成相关的基因。发现CTGF mRNA和蛋白水平被Cx26和GFP-Cx26下调。因此，我们的数据表明Cx26通过GJIC依赖性和非依赖性机制调节血管生成相关分子。

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